108268376 | Nucleic Acids are unique because | ability to direct their own replication from monomers. | |
108268377 | DNA Controls | biochemical, anatomical, physiological, and behavioral traits | |
108268378 | scientists use DNA to | change the heritable characteristics of a cell in laboratories | |
108268379 | Two chemical components of chromosomes | DNA & Proteins, proteins were stronger supported until 1940 | |
108268380 | DNA in heredity was first worked out by | studying bacteria and the viruses that infect them. | |
108268381 | People thought protein were basis due to | identified them as a class of macromolecules with great specificity of function. Nucleic acids weren't know: seemed far to uniform to account for inherited traits *chemical and physical* | |
108281612 | We can trace the genetic role of DNA to | 1928, fredrick griffith, studied bacterium that caused pneumonia in animals | |
108281613 | Griffith had.. | two strains of bacterium, a pathogenic and a nonpathogenic strain. | |
108281614 | Bacteria S | Smooth strain, pathogenic, because have a capsule that protects them from an animals defense system | |
108281615 | Bacteria R | Rought, strain lacked a capsule, and nonpathegonic. | |
108302192 | Results | S Cells: Died R Cells: Lived Heat killed S cells: Lived Mixture of heat-killed S sells and living R Cells: Died | |
108302193 | Griffiths conclusion: | living R bacteria had been transformed into pathogenic S by an unknown heritable substance from dead S cells | |
108302194 | Transformation | a change in genotype and phenotype due to the assimilation of external DNA by the cell. | |
108302195 | Descendants of the transformed bacteria | were all pathogenic. | |
108302196 | Oswald Avery | purified various types of molecules from the heat-killed pathogenic bacteria, then tried to transform live nonpathogenic bacteria with each type. DNA was transforming agent. | |
108361188 | Virus | Much simpler then cell, is just DNA enclosed in protective coat.To reproduce it must take over a cell. | |
108361189 | Viruses that attack bacteria | phages/bacteriophages | |
108373773 | Alfred Hershey and Martha Chase | experiments showed that DNA is the genetic material of a phage known as T2. | |
108373774 | During the time of this experiment: | 1) T2 was mostly DNA and protein 2) t2 phage could turn an ecoli cell in to a t2 producing factory | |
108373775 | Experiment Setup | Used radioactive phosphorus and Sulfer, mixed the elements with bacteria. Then they Put it in to a blender to separate phages outside the bacteria. Centrifuged the mixture. Then measured. | |
108373776 | Concluded that | DNA of the virus was injected into the host during infection, leaving the protein outside. the DNA produces more viruses. | |
113695154 | Chargaff | ATGC equal ammounts | |
113695155 | Thymine and Cytosine | one circle | |
113755593 | at/gc percents | AT = 30% GC = 19% | |
113886218 | When a cell copies a DNA molecule | each strand servers as a template for ordering nucleotides in to new, completmentary strands. | |
113886219 | DNA Replication basic | parent DNA has two complementary strands of DNA.First step of replication is breaking parent strand apart. Now each parent strand serves as a template that determines nulceotieds along a new complementary strand. Nucleotides are connected. Each consits of one parental and one new strand | |
113886220 | Semiconserivtive Model | when a double helix replicates, each of the two daugher molecules will have one old strand and one newly made strand. | |
113886221 | Conservative Model of Replication | parent molecules reform after the process. | |
113886222 | Dispersive Model | all four strands of DNA have a mixture of old and new DNA. | |
113939960 | Melson & Stahl | DNA follows semiconserivtive model. | |
113989900 | Orgins of Replication | Where Replication of DNA begins. | |
113989901 | Replication Fork | a y-shaped region where the new strands of DNA are elongating. at the end of replication buble. | |
114036178 | DNA Polymerases | Catalyze elongation of NEW DNA at replication form. Adds the nucleotides. | |
114066293 | The two strands of DNA in a double helix | are antiparralel | |
114066294 | New DNA strand can only | elongate in a 5->3 direction because DNA polymerases only add to the 3 end. | |
114066295 | Leading Strand | Made by DNA pol 3 adding nucleotides. | |
114066296 | Lagging strand | goes away from replication fork 3-> 5 diretion. | |
114066297 | Lagging strand | synthesized in a series of fragments. Once a replication buble opensfar enough, DNA pol 3 ataches to lagging strands template and moves away from replication fork. | |
114066298 | DNA Ligase (lagging strand) | Joins the oazaki fragments. | |
114143898 | DNA polymerase can't | inititate the synthessis of a polynucleotie. | |
114143900 | Primer | the initial nucleotide chain. | |
114143903 | Primase | starts RNA chain from scratch. Joins RNA nucleoties together one at a time. | |
114143906 | Okazaki fragments lagging strand | each must be primed seperately. | |
114143909 | Lagging strand synthesis | Primase joins RNA nucleotides in a primer. DNA POL 3 adds DNA NUCLEOTIDES TO THE PRIMER, forms okazaki fragment. Dna pol 3 adds dna nucleotides until it reaches the first primer. DNA pol 1 replaces the rna with dna. DNA ligase forms a bond between them. | |
114446304 | Telomers | Eukaryotic have them at the end. | |
114446305 | Telomers dont have | genes, instead the DNA consists of multiple repetitions of one short nucleotide sequence. | |
114446306 | Telomers dont | prevent the shortneing of DNA molecules, they just postpone the erosion of genes near the end of DNA molecules. |
AP BIO Chapter 16 Flashcards
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